Without evidence of benefit, an intervention should not be presumed to be beneficial or safe.

- Rogue Medic

2018 ACLS/PALS/NRP – AHA-ILCOR Guideline questions are being reviewed until 02-21-2017

AHA2015 - 2018
 

In preparation for the 2018 ACLS/PALS/NRP/CPR Guidelines (maybe 2017) the AHA (American Heart Association) and ILCOR (the International Liaison Committee On Resuscitation) are reviewing the questions they ask to examine the evidence, or the lack of evidence, on various interventions addressed by the guidelines for the:
 

First Aid Task Force (Public comment on PICO prioritization has recently closed. PICO categorization public comment period was open from October 10 to 24, 2016)

Advanced Life Support Task Force (Public comment on PICO categorization is NOW OPEN until 12:00 AM CST on February 21st, 2017!)

Basic Life Support Task Force (Public comment on PICO categorization is NOW OPEN until 12:00 AM CST on February 21st, 2017!)

Pediatric Life Support Task Force (Public comment on PICO categorization is NOW OPEN until 12:00 AM CST on February 21st, 2017!)

Education, Implementation and Teams Task Force (Public comment on PICO categorization is NOW OPEN until 12:00 AM CST on February 21st, 2017!)​

Neonatal Life Support Task Force (Public comment on PICO categorization is NOW OPEN until 12:00 AM CST on February 22nd, 2017!)[1]

 

Some questions are obvious and will be continued, such as 428. This is the review of antiarrhythmic drugs for cardiac arrest. Recent research shows no benefit to patients from amiodarone, or lidocaine.[2]

What do the 2015 ACLS Guidelines recommend?
 

Amiodarone may be considered for VF/pVT that is unresponsive to CPR, defibrillation, and a vasopressor therapy (Class IIb, LOE B-R).

Lidocaine may be considered as an alternative to amiodarone for VF/pVT that is unresponsive to CPR, defibrillation, and vasopressor therapy (Class IIb, LOE C-LD).[3]

 

Outside of controlled trials that are large enough to provide useful answers, amiodarone and lidocaine have no place in the treatment of cardiac arrest.
 

Much less obvious is 808, the suggestion that we should ventilate patients in the absence of evidence of benefit from ventilation – at least there is no evidence of benefit for the patient. Hands-only CPR seems to annoy doctors, nurses, paramedics, EMTs, . . . .

Why are we still ventilating adult cardiac arrest patients with cardiac causes of their cardiac arrest in the absence of evidence of safety and in the absence of evidence of benefit?
 

Why is there any question about 788? Results from Paramedic2 should be available next year. Is epinephrine in cardiac arrest better than a placebo?[4]

This is the first time we will have valid evidence to start to decide what to do with a treatment we have been using for over half a century based on the weakest of evidence. Paramedic2 is unlikely to answer many questions, such as which cardiac arrest patients should receive epinephrine and which should not, but it will be a start.
 

Then there is 464Drugs for monomorphic wide complex tachycardia. Considering the recent publication of PROCAMIO and the absence of discussion of tachycardia and bradycardia in the 2015 Guidelines, it is bizarre that this is among the questions recommended for elimination. Since there was no recommendation on treatment of ventricular tachycardia in the 2015 ACLS Guidelines, the recommendation from 2010 continues unchanged.

What did PROCAMIO show? If we give a high enough dose of amiodarone to actually try to treat the arrhythmia, major adverse cardiac events are more common than any benefit.[5]

Are we using amiodarone just to make stable ventricular tachycardia unstable?

Procainamide is safer and more effective.

Cardioversion is safer and more effective.

Adenosine is safer and probably more effective.[6]

Doing nothing is safer and only slightly less effective.

What about blood-letting for stable ventricular tachycardia?

Blood-letting is probably safer and maybe just as effective as amiodarone.[7]

Footnotes:

[1] ILCOR Continuous Evidence Evaluation
AHA (American Heart Association) and ILCOR (the International Liaison Committee On Resuscitation)
ILCOR 2016-2017 PICO categorization and prioritization public comment page

[2] Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest.
Kudenchuk PJ, Brown SP, Daya M, Rea T, Nichol G, Morrison LJ, Leroux B, Vaillancourt C, Wittwer L, Callaway CW, Christenson J, Egan D, Ornato JP, Weisfeldt ML, Stiell IG, Idris AH, Aufderheide TP, Dunford JV, Colella MR, Vilke GM, Brienza AM, Desvigne-Nickens P, Gray PC, Gray R, Seals N, Straight R, Dorian P; Resuscitation Outcomes Consortium Investigators..
N Engl J Med. 2016 May 5;374(18):1711-22. doi: 10.1056/NEJMoa1514204.
PMID: 27043165

Free Full Text from NEJM

[3] 2015 Recommendations—Updated
Part 7: Adult Advanced Cardiovascular Life Support
2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
2015 Recommendations—Updated

[4] Paramedic2 – The Adrenaline Trial
Warwick Medical School
About

[5] Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study.
Ortiz M, Martín A, Arribas F, Coll-Vinent B, Del Arco C, Peinado R, Almendral J; PROCAMIO Study Investigators.
Eur Heart J. 2016 Jun 28. pii: ehw230. [Epub ahead of print]
PMID: 27354046
 

The primary outcome, major adverse cardiac events within 40 minutes of infusion initiation, for procainamide vs. amiodarone, was 9% vs. 41%, p = 0.006. Severe hypotension or symptoms requiring immediate direct current cardioversion (DCCV) occurred in 6.3% vs. 31.0%. Results were similar in patients with structural heart disease (n = 49).

 

[6] Adenosine for wide-complex tachycardia – diagnostic?
Thu, 23 Aug 2012
Rogue Medic
Article

[7] Blood-Letting
Br Med J.
1871 March 18; 1(533): 283–291.
PMCID: PMC2260507
 

Physicians observed of old, and continued to observe for many centuries, the following facts concerning blood-letting.

1. It gave relief to pain. . . . .

2. It diminished swelling. . . . .

3. It diminished local redness or congestion. . . . .

4. For a short time after bleeding, either local or general, abnormal heat was sensibly diminished.

5. After bleeding, spasms ceased, . . . .

6. If the blood could be made to run, patients were roused up suddenly from the apparent death of coma. (This was puzzling to those who regarded spasm and paralysis as opposite states; but it showed the catholic applicability of the remedy.)

7. Natural (wrongly termed ” accidental”) hacmorrhages were observed sometimes to end disease. . . . .

8. . . . venesection would cause hamorrhages to cease.

 

.

The PROCAMIO Trial – IV Procainamide vs IV Amiodarone for the Acute Treatment of Stable Wide Complex Tachycardia

ResearchBlogging.org
 

This is a very interesting trial that may surprise the many outspoken amiodarone advocates, but it should not surprise anyone who pays attention to research.

ALPS showed that we should stop giving amiodarone for unwitnessed shockable cardiac arrest. The lead researcher is still trying to spin amiodarone for witnessed shockable cardiac arrest, even though the results do not show improvement in the one outcome that matters – leaving the hospital with a brain that still works.[1],[2],[3]

There is an excellent discussion of the study on the podcast by Dr. Salim Rezaie and Dr. Anand Swaminathan REBELCast: The PROCAMIO Trial – IV Procainamide vs IV Amiodarone for the Acute Treatment of Stable Wide Complex Tachycardia.

One problem with the study that they do not address on the podcast is that the patients in the study appear to have had time to watch Casablanca before treatment started. Here’s looking at you, while we’re waiting, kid. This is apparently unintentional one way of doing a placebo washout. If we wait long enough . . . .
 

Time from arrival to start of infusion was 87 ± 21 min for procainamide and 115 ± 36 min for amiodarone patients (P = 0.58).[4]

 

If nothing else, this demonstrates how little we need to worry about immediately pushing drugs for stable monomorphic VT (V Tach or Ventricular Tachycardia). Should we expect much from antiarrhythmic treatment?

Research shows that for stable monomorphic VT (V Tach or Ventricular Tachycardia) amiodarone is not very likely to be followed by an improvement. Only 29%[5] or only 25%[6] or only 15% within 20 minutes, but if we don’t mind waiting an hour it can be as much as 29%.[7] For those of you who are not good at math, that means amiodarone is about the same as doing nothing, only it comes in a syringe. Even though these poor outcomes ignore the side effects, they are the best evidence in favor of amiodarone, so what Kool-Aid are the advocates drinking?

Adenosine, yes adenosine the SVT (SupraVentricular Tachycardia) drug, appears to be more effective at treating ventricular tachycardia than amiodarone – and adenosine is faster and safer than amiodarone.[8]

What if the patient becomes unstable? First start an IV (IntraVenous) line. Then sedate the patient. Then apply defibrillator pads. After the patient is adequately sedated, then cardiovert. We do not need the pads on the patient first. If it takes a while to put the pads on, that is a problem with the ability of the doctors and nurses, not a medical problem.

It does not appear as if any patient received amiodarone or procainamide until after waiting in the ED (Emergency Department) for over an hour. Were some patients cardioverted in well under an hour? Probably. The important consideration is that the doctors and nurses be able to apply the defibrillator pads properly and quickly and deliver a synchronized cardioversion in less than a minute. If the patient has not yet been sedated, the cardioversion should be delayed until after the patient is adequately sedated, so the intervention that depends most on time is the sedation of the patient.
 

VT + Amiodarone Cardioversion
 

Is there a better treatment than amiodarone? Sedate the patient before the patient becomes unstable, then cardiovert. How do the MACEs (Major Adverse Cardiac Events) compare with sedation and cardioversion vs. antiarrhythmic treatment.
 

5.4 Proarrhythmia
Amiodarone may cause a worsening of existing arrhythmias or precipitate a new arrhythmia. Proarrhythmia, primarily torsade de pointes (TdP), has been associated with prolongation, by intravenous amiodarone, of the QTc interval to 500 ms or greater. Although QTc prolongation occurred frequently in patients receiving intravenous amiodarone, TdP or new-onset VF occurred infrequently (less than 2%). Monitor patients for QTc prolongation during infusion with amiodarone. Reserve the combination of amiodarone with other antiarrhythmic therapies that prolong the QTc to patients with life-threatening ventricular arrhythmias who are incompletely responsive to a single agent.
[9]

 

All antiarrhythmic drugs can cause arrhythmias. In the absence of information about a specific problem that is best addressed by a specific drug (amiodarone is the opposite of specific), we should avoid treatments that have such a high potential for harm.

Amiodarone doesn’t even do a good job of preventing arrhythmias.
 

Intravenous amiodarone did not prevent induction of sustained ventricular tachycardia in any of five patients inducible at baseline. Of six patients with non-sustained ventricular tachycardia, five had sustained ventricular tachycardia or fibrillation induced after amiodarone infusion.[10]

 

Is anything worse than amiodarone? Even epinephrine, yes epinephrine the inadequately tested cardiac arrest drug, has been followed by improved outcomes from V Tach after amiodarone failed.[11]
 

What is best for the patient?

Sedation, search for reversible causes, apply defibrillator pads, and be prepared to cardiovert.

Maybe sedation isn’t that important? This is by Dr. Peter Kowey, one of the top cardiologists in the world.
 

The man’s very first utterance was, “If it happens again, just let me die.”

As I discovered, the reason for this patient’s terror was that he had been cardioverted in an awake state. Ventricular tachycardia had been relatively slow, he had not lost consciousness, and the physicians, in the heat of the moment, had not administered adequate anesthesia. Although the 5 mg of intravenous diazepam had made him a bit drowsy, he felt the electric current on his chest and remembered the event clearly.

The patient’s mental state complicated the case considerably.[12]

 

How unimportant is sedation? How unimportant is consent?

For sedation, I would recommend ketamine, but etomidate was recommended in the podcast. Both work quickly and the most important obstacle to immediate treatment of a patient who suddenly deteriorates is the time to effect of sedation. Neither drug is expected to interfere with perfusion, which is the main excuse given for avoiding sedation for cardioversion.

This study is very small (not the fault of the authors), but it adds to the evidence that amiodarone is not a good first treatment for the patient.
 

Go listen to the podcast by Dr. Salim Rezaie and Dr. Anand Swaminathan REBELCast: The PROCAMIO Trial – IV Procainamide vs IV Amiodarone for the Acute Treatment of Stable Wide Complex Tachycardia

 

Over the years, I have written a bit about cardioversion and the importance of sedation –

Cardioversion – I’m not doing that, you do it! – Mon, 24 Mar 2008

Cardioversion – 2010 ACLS – Part I – Mon, 25 Oct 2010

Cardioversion – 2010 ACLS – Part II – Sun, 31 Oct 2010

Cardioversion – 2010 ACLS – Part III – Thu, 11 Nov 2010

On the relative wisdom of synchronized cardioversion without sedation – Part I – Thu, 11 Nov 2010

On the relative wisdom of synchronized cardioversion without sedation – Part II – Fri, 12 Nov 2010

Synchronized Cardioversion Without Sedation – Part II Scallywag’s Response – Sun, 14 Nov 2010

On the relative wisdom of synchronized cardioversion without sedation – Part III – Tue, 16 Nov 2010

On the relative wisdom of synchronized cardioversion without sedation – Part IV – Wed, 24 Nov 2010

Comments on Cardioversion – 2010 ACLS – Part II – Mon, 16 Apr 2012
 

I have also written a bit about amiodarone –

Merit Badge Courses, Amiodarone, and tPA – Fri, 17 Sep 2010

Amiodarone for Cardiac Arrest in the 2010 ACLS – Part I – Wed, 01 Dec 2010

Amiodarone for Cardiac Arrest in the 2010 ACLS – Part II – Fri, 03 Dec 2010

Is Nexterone the Next Amiodarone? – Sat, 04 Dec 2010

Amiodarone for Cardiac Arrest in the 2010 ACLS – Part III – Mon, 06 Dec 2010

Where are the Black Box Warnings on These Drugs – I – Mon, 05 Dec 2011

Where are the Black Box Warnings on These Drugs – II – Sun, 11 Dec 2011

Is Amiodarone the Best Drug for Stable Ventricular Tachycardia – Wed, 14 Dec 2011

V Tach Storm – Part I – Wed, 28 Dec 2011

V Tach Storm – Part II – Thu, 29 Dec 2011

Nifekalant versus lidocaine for in-hospital shock-resistant ventricular fibrillation or tachycardia – Wed, 04 Jan 2012

NIH launches trials to evaluate CPR and drugs after sudden cardiac arrest – Sun, 29 Jan 2012

What Will Be the Next Standard Of Care We Eliminate – Wed, 28 Mar 2012

Happy Adenosine Day – Tue, 12 Jun 2012

Too Much Medicine and Evidence-Based Guidelines – Part I – Tue, 26 Jun 2012

Too Much Medicine and Evidence-Based Guidelines – Part II – Tue, 03 Jul 2012

Ondansetron (Zofran) Warning for QT Prolongation – is Amiodarone next? – Part I – Mon, 02 Jul 2012

Ondansetron (Zofran) Warning for QT Prolongation – is Amiodarone next? – Part II – Thu, 05 Jul 2012

Wide variability in drug use in out-of-hospital cardiac arrest: A report from the resuscitation outcomes consortium – Part I – Mon, 17 Sep 2012

Wide variability in drug use in out-of-hospital cardiac arrest: A report from the resuscitation outcomes consortium – Part II – Tue, 18 Sep 2012

How do we measure the QT segment when there are prominent U waves? – Thu, 13 Dec 2012

Woman with Risks for Torsades de Pointes Dying within Hours of Leaving the Emergency Department – Wed, 02 Jan 2013

Examples of Ventricular Tachycardia Caused by Amiodarone – Part I – Tue, 28 May 2013

Publication Bias – The Lit Whisperers – Tue, 11 Jun 2013

Standards Of Care – Ventricular Tachycardia – Wed, 31 Jul 2013

Footnotes:

[1] Dr. Kudenchuk is Misrepresenting ALPS as ‘Significant’
Tue, 12 Apr 2016
Rogue Medic
Article

[2] Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest
Mon, 04 Apr 2016
Rogue Medic
Article

[3] Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest.
Kudenchuk PJ, Brown SP, Daya M, Rea T, Nichol G, Morrison LJ, Leroux B, Vaillancourt C, Wittwer L, Callaway CW, Christenson J, Egan D, Ornato JP, Weisfeldt ML, Stiell IG, Idris AH, Aufderheide TP, Dunford JV, Colella MR, Vilke GM, Brienza AM, Desvigne-Nickens P, Gray PC, Gray R, Seals N, Straight R, Dorian P; Resuscitation Outcomes Consortium Investigators.
N Engl J Med. 2016 May 5;374(18):1711-22. doi: 10.1056/NEJMoa1514204. Epub 2016 Apr 4.
PMID: 27043165

CONCLUSIONS
Overall, neither amiodarone nor lidocaine resulted in a significantly higher rate of survival or favorable neurologic outcome than the rate with placebo among patients with out-of-hospital cardiac arrest due to initial shock-refractory ventricular fibrillation or pulseless ventricular tachycardia.

[4] Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study.
Ortiz M, Martín A, Arribas F, Coll-Vinent B, Del Arco C, Peinado R, Almendral J; PROCAMIO Study Investigators.
Eur Heart J. 2016 Jun 28. pii: ehw230. [Epub ahead of print]
PMID: 27354046

Free Full Text from European Heart Journal.

[5] Amiodarone or procainamide for the termination of sustained stable ventricular tachycardia: an historical multicenter comparison.
Marill KA, deSouza IS, Nishijima DK, Senecal EL, Setnik GS, Stair TO, Ruskin JN, Ellinor PT.
Acad Emerg Med. 2010 Mar;17(3):297-306.
PMID: 20370763 [PubMed – indexed for MEDLINE]

Free Full Text from Academic Emergency Medicine.

[6] Amiodarone is poorly effective for the acute termination of ventricular tachycardia.
Marill KA, deSouza IS, Nishijima DK, Stair TO, Setnik GS, Ruskin JN.
Ann Emerg Med. 2006 Mar;47(3):217-24. Epub 2005 Nov 21.
PMID: 16492484 [PubMed – indexed for MEDLINE]

[7] Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment?
Tomlinson DR, Cherian P, Betts TR, Bashir Y.
Emerg Med J. 2008 Jan;25(1):15-8.
PMID: 18156531 [PubMed – indexed for MEDLINE]

[8] Adenosine for wide-complex tachycardia – diagnostic?
Thu, 23 Aug 2012
Rogue Medic
Article

[9] AMIODARONE HYDROCHLORIDE- amiodarone hydrochloride injection, solution
DailyMed
5 WARNINGS AND PRECAUTIONS
FDA Label

[10] Effects of intravenous amiodarone on ventricular refractoriness, intraventricular conduction, and ventricular tachycardia induction.
Kułakowski P, Karczmarewicz S, Karpiński G, Soszyńska M, Ceremuzyński L.
Europace. 2000 Jul;2(3):207-15.
PMID: 11227590 [PubMed – indexed for MEDLINE]

Free Full Text PDF + HTML from Europace

[11] Low doses of intravenous epinephrine for refractory sustained monomorphic ventricular tachycardia.
Bonny A, De Sisti A, Márquez MF, Megbemado R, Hidden-Lucet F, Fontaine G.
World J Cardiol. 2012 Oct 26;4(10):296-301. doi: 10.4330/wjc.v4.i10.296.
PMID: 23110246 [PubMed]

Free Full Text from PubMed Central.

[12] The calamity of cardioversion of conscious patients.
Kowey PR.
Am J Cardiol. 1988 May 1;61(13):1106-7. No abstract available.
PMID: 3364364

Kudenchuk PJ, Brown SP, Daya M, Rea T, Nichol G, Morrison LJ, Leroux B, Vaillancourt C, Wittwer L, Callaway CW, Christenson J, Egan D, Ornato JP, Weisfeldt ML, Stiell IG, Idris AH, Aufderheide TP, Dunford JV, Colella MR, Vilke GM, Brienza AM, Desvigne-Nickens P, Gray PC, Gray R, Seals N, Straight R, Dorian P, & Resuscitation Outcomes Consortium Investigators (2016). Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest. The New England journal of medicine, 374 (18), 1711-22 PMID: 27043165

Ortiz M, Martín A, Arribas F, Coll-Vinent B, Del Arco C, Peinado R, Almendral J, & PROCAMIO Study Investigators (2016). Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study. European heart journal PMID: 27354046

Marill KA, deSouza IS, Nishijima DK, Senecal EL, Setnik GS, Stair TO, Ruskin JN, & Ellinor PT (2010). Amiodarone or procainamide for the termination of sustained stable ventricular tachycardia: an historical multicenter comparison. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 17 (3), 297-306 PMID: 20370763

Marill KA, deSouza IS, Nishijima DK, Stair TO, Setnik GS, & Ruskin JN (2006). Amiodarone is poorly effective for the acute termination of ventricular tachycardia. Annals of emergency medicine, 47 (3), 217-24 PMID: 16492484

Tomlinson DR, Cherian P, Betts TR, & Bashir Y (2008). Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment? Emergency medicine journal : EMJ, 25 (1), 15-8 PMID: 18156531

Kułakowski P, Karczmarewicz S, Karpiński G, Soszyńska M, & Ceremuzyński L (2000). Effects of intravenous amiodarone on ventricular refractoriness, intraventricular conduction, and ventricular tachycardia induction. Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology, 2 (3), 207-15 PMID: 11227590

Bonny A, De Sisti A, Márquez MF, Megbemado R, Hidden-Lucet F, & Fontaine G (2012). Low doses of intravenous epinephrine for refractory sustained monomorphic ventricular tachycardia. World journal of cardiology, 4 (10), 296-301 PMID: 23110246

Kowey PR (1988). The calamity of cardioversion of conscious patients. The American journal of cardiology, 61 (13), 1106-7 PMID: 3364364

.

1-Union-801 Podcast Discussing Epi for V Tach, Cardioversion, Procainamide, Paralytics During Hypothermia, Quality of CPR, and DNA Transfer


 

 
On 1-Union-801 John Broyles and I discussed some things that I had written. I was supposed to be on the podcast two weeks earlier, but I am on duty at the time of the podcast, and I had a call a few minutes before the show. This podcast was not interrupted by any calls.[1]
 

Go listen to the podcast.
 

Epinephrine for V Tach – Instant Death or Effective Treatment?

What might happen if epinephrine is given for this V Tach (Ventricular Tachycardia)?
 

Click on images to make them larger. Image credit and article about epinephrine for V Tach.[2]
 

We also discuss sychronized cardioversion and procainamide.
 
Other things we discussed (in order) were –

Do Paralytics Improve Outcomes Following Resuscitation?

We want to minimize movement after starting therapeutic hypothermia. Is the use of paralytics the right way to do this?
 

Un-extraordinary measures: Stats show CPR often falls flat

The author appears to take the comments of Dr. David Newman completely out of context in order to make a point that I do not think Dr. Newman would ever make.

Who is Dr. Newman?
 

 

SMART EM

Dr. David Newman, and sometimes Dr. Ashley Shreves, write and podcast about research and emergency medicine. There is an excellent deconstruction of the ACLS (Advanced Cardiac Life Support) guidelines and the lack of evidence for the drugs recommended in the guidelines.

The NNT is another excellent site that is here, too.

At Annals of Emergency Medicine, Dr. Newman and Dr. Ashley Shreves present excellent summaries of the articles in each issue. Annals of Emergency Medicine Podcast

I also mentioned Dr. Richard Levitan’s No Desat approach of using high flow oxygen by nasal cannula, which works wonders. Read about No Desat!
 

Apparent DNA Transfer by Paramedics Leads to Wrongful Imprisonment

Do we use gloves properly?

Is DNA transfer between patients an indication of a lack of use of gloves?
 

Go listen to the podcast.
 

Footnotes:

[1] Rogue Medic Saved Our Bacon 20 Jul 13
1-Union-801
John Broyles
Podcast page.

[2] Low doses of intravenous epinephrine for refractory sustained monomorphic ventricular tachycardia.
Bonny A, De Sisti A, Márquez MF, Megbemado R, Hidden-Lucet F, Fontaine G.
World J Cardiol. 2012 Oct 26;4(10):296-301. doi: 10.4330/wjc.v4.i10.296.
PMID: 23110246 [PubMed]

Free Full Text from PubMed Central.

.

V Tach Storm – Part II


Continuing from Part I.

What is amiodarone?

Mechanism of Action
Amiodarone is generally considered a class III antiarrhythmic drug, but it possesses electrophysiologic characteristics of all four Vaughan Williams classes.
[1]

If you use ventilators, do you change all of the settings at once, or do you adjust one at a time? Amiodarone changes all of the conduction at the same time, just not in ways that are as controllable as the settings on a ventilator.


Image credit.

Amiodarone is the napalm of antiarrhythmics. Amiodarone hits everything all at once. Amiodarone interferes with all of the Vaughn Williams classes. Some people think that a broad-spectrum antiarrhythmic is somehow a good thing. That might be the case, if there were a reason to believe that the patient is experiencing problems with all 4 of these conduction systems and the amiodarone is going to improve all 4 of these conduction systems.

What are the chances of that?

Imagine trying to guess the combination to a very simple 4 digit combination lock. We will make the digits binary, since the choices are more conduction or less conduction. No change is not really a possibility with amiodarone. How would we calculate the odds of reaching the right combination?

Each class has only 2 possibilities, so the calculation is 2 X 2 X 2 X 2 = 16. [2] Four different conduction systems being manipulated – all at the same time.

But it isn’t even that complicated. We know what the expected direction of effect of the amiodarone will be. The only question is whether the effect of amiodarone makes things better for that class, or if amiodarone makes things worse. This is still a binary consideration, so the calculation does not change.

Of course, this is an over-simplification, but Just give amiodarone is also an over-simplification.

He’s got an odd rhythm on the ECG.

Just give amiodarone.

Don’t you want to know what the rhythm is?

Just give amiodarone.

But what if amiodarone makes things worse?

Just give amiodarone.

As simple as pointing a diagnostic device and pressing Go or pointing at a drug and grunting. 21st Century Emergency Medical Care.

If amiodarone is so good, why do so many patients end up being cardioverted?

For monomorphic V Tach – less than 30% success[3],[4],[5] – and monomorphic V Tach is what amiodarone is best at.

If amiodarone is safe, that may not be a bad idea, but . . . .

Pharmacodynamics
Amiodarone I.V. has been reported to produce negative inotropic and vasodilatory effects in animals and humans. In clinical studies of patients with refractory VF or hemodynamically unstable VT, treatment-emergent, drug-related hypotension occurred in 288 of 1836 patients (16%) treated with amiodarone I.V. No correlations were seen between the baseline ejection fraction and the occurrence of clinically significant hypotension during infusion of amiodarone I.V.
[1]

16% develop hypotension?

Isn’t hypotension one of the things we are trying to avoid?

Yes.

Less than 30% improve, but 16% get worse?

Maybe that is why the FDA (Food and Drug Administration) label only says that we should be using amiodarone after other treatments do not work.

INDICATIONS AND USAGE
Amiodarone HCI Injection is indicated for initiation of treatment and prophylaxis of frequently recurring ventricular fibrillation and hemodynamically unstable ventricular tachycardia in patients refractory to other therapy.
[1]

Amiodarone may not be a good starting point for treatment, but more of a last ditch – It can’t possibly get any worse, so what has the patient got to lose? treatment.

In Dr. Orman’s podcast – V Tach Storm – hemodynamically unstable is where the patient ended up after amiodarone. The patient’s heart rate is 207, but he is hypertensive. 150 mg of amiodarone is reported to have been given over 5 to 10 minutes, even though ACLS and the FDA label state that the initial dose should be given over 10 minutes. He later repeats the dose of amiodarone and adds 2 gm magnesium. A couple of sinus beats emerged, but went away, but now his heart rate is over 220.

Dr. Orman states, “You’re making some headway. Probably what you are doing is having some effect on him, but it’s not quite getting you where you want to go.”

The patient becomes hypotensive – from 175 systolic to 90/55 and he became short of breath. Is it the amiodarone, or the magnesium, or the rhythm, or something else, or some combination of these?

Then he appears to have been given some propofol for sedation and cardioverted at 200 joules, then 300 joules, then 360 joules. The doctor feels the need to apologize for repeating cardioversion, which I don’t understand. Why not sedate and cardiovert earlier?

My experience has been that cardioversion is frequently done incorrectly. That is one of the reasons I would spend a lot of time on cardioversion in ACLS classes. The ACLS procedures most commonly fouled uo are cardioversion, transcutaneous pacing, needle decompression of tension pneumothorax, and needle decompression of cardiac tamponade.

Not many people are comfortable cardioverting patients.

Eventually, the cardiologist gave another 150 mg of amiodarone and 5 mg of metoprolol and soon after the arrhythmia changed to a 50/50 mix of sinus tachycardia and V Tach.


Click on the image to make it larger.

A stable 75 year old patient with V Tach at a rate of almost 200. An unknown dose of disopyramide (Norpace), 135 mg lidocaine, cardioversion X 4, 150 mg amiodarone, 2 gm magnesium, 150 mg amiodarone, an unknown dose of propofol, cardioversion X 3, 150 mg amiodarone, and 5 mg metoprolol. After deterioration, he improves to an alternating V Tach and sinus tachycardia with each present about half of the time.

How much did the drugs help?

How much did the drugs hurt?

We do not know.

Procainamide was not given. Sotalol was given in the ICU.

The patient was taking disopyramide (Norpace), which is mentioned as being proarrhythmic, but lidocaine is proarrhythmic. Amiodarone is proarrhythmic. Why are the proarrhythmic effects of these drugs not also mentioned?

When do we stop throwing proarrhythmic medications at a rhythm?

At the end, there is a good discussion of other possible treatments, which you should listen to. V Tach Storm.

Footnotes:

[1] AMIODARONE HYDROCHLORIDE injection, solution
[Bedford Laboratories]

FDA label
Label

Like class I drugs, amiodarone blocks sodium channels at rapid pacing frequencies, and like class II drugs, it exerts a noncompetitive antisympathetic action. One of its main effects, with prolonged administration, is to lengthen the cardiac action potential, a class III effect. The negative chronotropic effect of amiodarone in nodal tissues is similar to the effect of class IV drugs. In addition to blocking sodium channels, amiodarone blocks myocardial potassium channels, which contributes to slowing of conduction and prolongation of refractoriness. The antisympathetic action and the block of calcium and potassium channels are responsible for the negative dromotropic effects on the sinus node and for the slowing of conduction and prolongation of refractoriness in the atrioventricular (AV) node. Its vasodilatory action can decrease cardiac workload and consequently myocardial oxygen consumption.

[2] Here is a list of the possibilities, for those wanting to see the math.

1. BetterBetterBetterBetter.

2. BetterBetterBetter – Worse.

3. BetterBetter – Worse – Better.

4. Better – Worse – BetterBetter.

5. Worse – BetterBetterBetter.

6. BetterBetter – Worse – Worse.

7. Better – Worse – Better – Worse.

8. Worse – BetterBetter – Worse.

9. Better – Worse – Worse – Better.

10. Worse – Better – Worse – Better.

11. Worse – Worse – BetterBetter.

12. Better – Worse – Worse – Worse.

13. Worse – Better – Worse – Worse.

14. Worse – Worse – Better – Worse.

15. Worse – Worse – Worse – Better.

16. Worse – Worse – Worse – Worse.

[3] Amiodarone is poorly effective for the acute termination of ventricular tachycardia.
Marill KA, deSouza IS, Nishijima DK, Stair TO, Setnik GS, Ruskin JN.
Ann Emerg Med. 2006 Mar;47(3):217-24. Epub 2005 Nov 21.
PMID: 16492484 [PubMed – indexed for MEDLINE]

[4] Amiodarone or procainamide for the termination of sustained stable ventricular tachycardia: an historical multicenter comparison.
Marill KA, deSouza IS, Nishijima DK, Senecal EL, Setnik GS, Stair TO, Ruskin JN, Ellinor PT.
Acad Emerg Med. 2010 Mar;17(3):297-306.
PMID: 20370763 [PubMed – indexed for MEDLINE]

Free Full Text from Academic Emergency Medicine.

[5] Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment?
Tomlinson DR, Cherian P, Betts TR, Bashir Y.
Emerg Med J. 2008 Jan;25(1):15-8.
PMID: 18156531 [PubMed – indexed for MEDLINE]

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V Tach Storm – Part I


In the comments to Is Amiodarone the Best Drug for Stable Ventricular Tachycardia is the following from Doc Cottle of Mill Hill Ave Command.

I just gave procainamide in the ER a few weeks ago, partly because it seemed like the best drug for the odd situation, but also just to get people back into the habit of using it. When a trauma/CC surgeon heard I was giving it, he said “You’re not old enough to give procainamide!”

Unfortunately, I would not be on the receiving end of that comment, for age or procainamide. My adult wide complex tachycardia protocol does not include procainamide. My pediatric wide complex tachycardia protocol does include procainamide. Go figure.

It would be nice to have an antiarrhythmic that is significantly more effective than placebo. I do not think that we have good evidence that amiodarone, or lidocaine, is really any better than placebo. Less than 30% effective at terminating stable monomorphic V Tach (VT or Ventricular Tachycardia) does not exactly suggest effective. Causing hypotension, bradycardia, torsades, and other arrhythmias does not exactly suggest safe.

Well, stick around long enough, and the passe becomes hip again.

Calcium chloride, too.

By the way, you might appreciate Rob Orman’s podcast ERCAST, where he talks about treating refractory VT. (http://blog.ercast.org/2010/12/v-tach-storm/)

V Tach Storm is an important podcast, but I have a few problems with what is covered.

The topic is –

 

What do we do when we run out of algorithm?

 

I don’t think that should be the question. I think that we have become too protocol driven, but that is part of what Dr. Orman describes.

The question is Why is the patient experiencing this arrhythmia?

We can get rid of arrhythmias without addressing the underlying cause. With some treatments, we exacerbate the underlying cause.

What was done for/to the patient?

PS – The age is cut off at the beginning of the podcast. The patient is 75 years old. EMS initially gave lidocaine, then shocked him without any sedation, even though he had stable vital signs and should have been given sedation. Even if the patient hypotension, ketamine would have been a good sedative, but few of us in EMS have ketamine.

 

Shocked four times without sedation.

 

Ouch!

 

Then, amiodarone was given, even though amiodarone is not a drug that consistently produces good outcomes. For a baseball player, a batting average of .290 is not bad. For a drug, .290 is only good if there are no better alternatives and the drug is safe.

Studies show that amiodarone is only 29% effective at terminating V Tach,[1] only 25% effective at terminating V Tach, [2], and only 15% effective at terminating V Tach within 20 minutes, but if we don’t mind waiting an hour it can be as much as 29% effective.[3]

If we are not trying to convert the rhythm promptly, should we even consider V Tach an emergency? If lights and sirens only make a difference of a minute, or two, V Tach is obviously not a lights and sirens emergency. Maybe we need a treatment that works.

At least amiodarone doesn’t cause arrhythmias. Right?

Intravenous amiodarone did not prevent induction of sustained ventricular tachycardia in any of five patients inducible at baseline. Of six patients with non-sustained ventricular tachycardia, five had sustained ventricular tachycardia or fibrillation induced after amiodarone infusion.[4]

Of 6 patients with non-sustained V Tach, 5 of them developed sustained V Tach or developed V Fib (Ventricular Fibrillation). In what way does amiodarone seem like a good idea?

Is amiodarone safe?

As long as we don’t mind causing hypotension, causing bradycardia, converting non-sustained V Tach to sustained V Tach, causing torsades, and causing V Fib. We wouldn’t hold those really bad things against amiodarone.

Continued in Part II.

Footnotes:

[1] Amiodarone is poorly effective for the acute termination of ventricular tachycardia.
Marill KA, deSouza IS, Nishijima DK, Stair TO, Setnik GS, Ruskin JN.
Ann Emerg Med. 2006 Mar;47(3):217-24. Epub 2005 Nov 21.
PMID: 16492484 [PubMed – indexed for MEDLINE]

[2] Amiodarone or procainamide for the termination of sustained stable ventricular tachycardia: an historical multicenter comparison.
Marill KA, deSouza IS, Nishijima DK, Senecal EL, Setnik GS, Stair TO, Ruskin JN, Ellinor PT.
Acad Emerg Med. 2010 Mar;17(3):297-306.
PMID: 20370763 [PubMed – indexed for MEDLINE]

Free Full Text from Academic Emergency Medicine.

[3] Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment?
Tomlinson DR, Cherian P, Betts TR, Bashir Y.
Emerg Med J. 2008 Jan;25(1):15-8.
PMID: 18156531 [PubMed – indexed for MEDLINE]

[4] Effects of intravenous amiodarone on ventricular refractoriness, intraventricular conduction, and ventricular tachycardia induction.
Kułakowski P, Karczmarewicz S, Karpiński G, Soszyńska M, Ceremuzyński L.
Europace. 2000 Jul;2(3):207-15.
PMID: 11227590 [PubMed – indexed for MEDLINE]

Free Full Text PDF + HTML from Europace

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Where are the Black Box Warnings on These Drugs – II

Continuing with the answer to Where are the Black Box Warnings on These Drugs – I.

There is a black box warning on droperidol for prolonging the QT segment, but there is no black box warning for this commonly used EMS drug (Drug X) that also prolongs the QT segment. Are we supposed to think that Drug X is safer than droperidol?

What is Drug X?

Proarrhythmia
Like all antiarrhythmic agents, amiodarone I.V. may cause a worsening of existing arrhythmias or precipitate a new arrhythmia. Proarrhythmia, primarily torsades de pointes (TdP), has been associated with prolongation by amiodarone I.V. of the QTc interval to 500 ms or greater. Although QTc prolongation occurred frequently in patients receiving amiodarone I.V., torsades de pointes or new-onset VF occurred infrequently (less than 2%). Patients should be monitored for QTc prolongation during infusion with amiodarone I.V. Combination of amiodarone with other antiarrhythmic therapy that prolongs the QTc should be reserved for patients with life-threatening ventricular arrhythmias who are incompletely responsive to a single agent.
[1]

Have you ever been warned about the possibility of inducing torsades de pointes or new-onset VF with amiodarone?

What is the incidence of torsades de pointes or new-onset VF with droperidol?

Much much less than 2%.

Although QTc prolongation occurred frequently in patients receiving amiodarone I.V., torsades de pointes or new-onset VF occurred infrequently (less than 2%). Patients should be monitored for QTc prolongation during infusion with amiodarone I.V.

Where is the black box warning for amiodarone for more frequent torsades and VF?


VT source. Torsades source.

Maybe you have not seen torsades even with semi-frequent administration of amiodarone.

How many people have seen torsades even with more frequent administration of droperidol?

Electrolyte Disturbances
Patients with hypokalemia or hypomagnesemia should have the condition corrected whenever possible before being treated with amiodarone I.V., as these disorders can exaggerate the degree of QTc prolongation and increase the potential for TdP. Special attention should be given to electrolyte and acid-base balance in patients experiencing severe or prolonged diarrhea or in patients receiving concomitant diuretics.
[1]

Have you ever been warned to avoid giving amiodarone to hypokalemic or hypomagnesemic patients?

In EMS, other than guessing based on the patient’s history, how would we know that the patient has hypokalemia or hypomagnesemia?

In the ED (Emergency Department), are magnesium or potassium levels checked before giving amiodarone?

 

Why does droperidol have a black box warning?

 

Amiodarone is associated with more frequent torsades and VF than droperidol.

We give out amiodarone more often than banks give political donations.

 

Why doesn’t amiodarone have a black box warning?

 

Footnotes:

[1] AMIODARONE HYDROCHLORIDE injection, solution
[Bedford Laboratories]

FDA label
Label

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Potentially Reversible Causes of Cardiac Arrest – Arrhythmia

In my last post, Not Successful Resuscitation, I mentioned the potentially reversible causes of cardiac arrest. First a definition. These are conditions that can lead to sudden death as well as a more gradual death. In the case of a more gradual death, their potential for reversibility dramatically decreases. One of the reasons is that these conditions, conditions bad enough to kill you, can cause significant organ damage when they are present for an extended period. Acidosis is very destructive to the body, but if it is a sudden change, rather than a long term condition (especially one that is not responding to aggressive medical treatment), then reversing the acidosis may help to resuscitate the patient.

Why only may?

There are many factors that affect the ability to resuscitate a patient. As I mentioned, a gradual onset is not as easy to reverse. A gradual onset is because the illness is a chronic condition or a progressive condition.

But if it is a progressive condition, that has progressed to death, how can it be a reversible cause of cardiac arrest?

The potentially reversible causes tend to be sudden. That does not mean that a gradual onset rules out resuscitation, just that it becomes much more difficult to resuscitate these patients, and much more difficult to keep these patients alive if we do manage to resuscitate them. These causes tend to be overwhelming to the body. Still, a sudden onset of a potentially reversible cause of cardiac arrest may not respond to treatment, even if the patient is in the ideal treatment setting, because these causes are only potentially reversible.

Then why spend so much time on them?

All of resuscitation is about potentially reversible causes. VF/Pulseless VT (Ventricular Fibrillation/Pulseless Ventricular Tachycardia) are the easiest to reverse, the most likely to be reversed, and the easiest to diagnose.

Diagnose? Paramedics can’t diagnose.

Of course you can. You just can’t legally claim that you are diagnosing. This is purely a legal distinction. It has no basis in reality.

Arrhythmia – shocking a shockable rhythm.

Some of the arrhythmias that can cause cardiac arrest may be reversed by defibrillation. Some of the arrhythmias that can cause cardiac arrest will not improve with defibrillation. Asystole is an excellent example of an arrhythmia that will not respond to defibrillation. Asystole is caused by defibrillation. We shock patients because we want to cause asystole – temporarily.

The defibrillation is designed to send enough current through the heart to stop the heart for less than a second. The purpose of defibrillation is to get rid of the dangerous rhythm that is controlling the heart, whether it is an organized rhythm, such as VT or SVT (SupraVentricular Tachycardia), or disorganized activity, such as VF.

After the shock is delivered, and some asystole is produced, it is hoped that the heart starts again on its own and when the heart starts again, it is hoped that the sinus node will be controlling the rate and rhythm. If the patient’s normal pacemaker is not the sinus node (a couple of examples are atrial fibrillation or an implanted pacemaker), then the hope is that the normal pacemaker resumes its role of initiating a rhythm capable of keeping the patient alive.

In western movies, during a big bar fight, the sheriff may fire a gun into the air. Everyone tends to stop, at least long enough to make sure the gun is not pointed at them. This pause in the commotion is what defibrillation is supposed to accomplish. The sheriff is telling the arrhythmia to move along. As in the movies, it does not always work as planned. If the arrhythmia/chaos does not go away with defibrillation, more defibrillation may be attempted. Even if the ceiling is shot full of defibrillations, there is no maximum number of defibrillations, as long as the patient is in a shockable rhythm. Antiarrhythmic medications may be added to the treatment (after some epinephrine, the most arrhythmogenic drug we use). The search for other potentially reversible causes of cardiac arrest will contribute to treatment.

Arrhythmogenic?

Something that causes arrhythmias. I describe problems with the use of epinephrine in Epinephrine in Cardiac Arrest, More on Epinephrine in Cardiac Arrest, and Dead VT vs Not Quite Dead, Yet VT.

What if the asystole is not temporary?

This is not unusual. The current ACLS (Advanced Cardiac Life Support) algorithms are pretty easy to use.[1] If you are using an algorithm that no longer applies, you should switch to the algorithm that does apply. I will cover asystole in another post.

Are there any other rhythms that should be defibrillated?

SVT – if the patient is pulseless. Any rhythm that would be cardioverted, if the patient were alive, should be defibrillated if the rhythm is bad enough to produce a dead patient. Although this falls into the category of PEA (Pulseless Electrical Activity), it is a shockable rhythm and will respond best to defibrillation.

One of the perversions of the algorithms is that they spend almost no time on Postresuscitation Support. There is no algorithm, flow sheet, or other easy to use chart. The 2010 ACLS Guidelines added an easy to use algorithm.[2] This is the AHA (American Heart Association), in the 2000 guidelines they were not discouraged by the possibility of an overly dense, extremely confusing 3 page tachycardia algorithm “overview” flow sheet. Pages 1, 2, and 3, followed by the individual pages for specific tachyarrhythmias. Fortunately they did learn from that, but there is still no algorithm to ease recall of postresuscitation care – something that is not well understood. That will be more than another post.

There are methods of determining if the arrest is one that may be reversed by treatment. Again, this is something for another post.

That is enough of the potentially reversible causes for this post. And I haven’t even started on the list of potentially reversible causes. 🙂

The PALS (Pediatric Advanced Life Support) potentially reversible causes of cardiac arrest list is 5 H’s and 5 T’s:

Hypovolemia; Hypoxia; Hydrogen ion (Acidosis); Hypo/Hyperkalemia; Hypoglycemia; Hypothermia.

Toxins (Drugs); Tamponade, cardiac; Tension pneumothorax; Thrombosis (coronary or pulmonary – AMI or PE); Trauma

I have changed this from what I originally wrote. My, borrowed from Jeff B of JB on the Rocks, mnemonic (memory aid) for the potentially reversible causes of cardiac arrest is now two words – COLD PATCHeD.

COLD reminds you that the C is for hypothermia – being very cold, sometimes we forget the obvious in resuscitation attempts, so it doesn’t hurt to put extra reminders in a mnemonic. O for Oxygen deficit or hypoxia. L for Lytes. This works better as a mnemonic for the in hospital crowd, but there is nothing wrong with getting EMS to think more about electroLytes. Hypokalemia and Hyperkalemia – too little and too much potassium. D for Drugs (OverDose, poison, wrong drug, wrong dose, . . .).

PATCHeD = PPE (Pulmonary Embolus); A Acidosis and AMI (Acute Myocardial Infarction); T Tension Pneumothorax; C – Cardiac Tamponade; H – Here it is still confusing, a whole bunch of Hypo’s and one Hyper. The Hypo’s: HypoVolemia; HypoThermia; HypoGlycemia; HypOxia; HypoKalemia; The Hyper: HyperKalemia; e – Everybody dead gets Epi. Just a reminder to continue CPR and other treatments. D Drugs (OD, poison, wrong drug, wrong dose, . . .); Distributive Shock.

I will have to write a post on why each of these categories matter, what the treatments are, and other ways to approach them, rather than the order of the mnemonic. This is a lot for one post.

Footnotes:

[1] 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science
Volume 122, Issue 18_suppl_3;
November 2, 2010
Guidelines index

Below is the link to the old guidelines:

2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Volume 112, Issue 24 Supplement;
December 13, 2005
Guidelines index

[2] Post–cardiac arrest care algorithm.
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 9: Post–Cardiac Arrest Care
Systems of Care for Improving Post–Cardiac Arrest Outcomes
Algorithm in JPEG format

Part 9: Post–Cardiac Arrest Care
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Free Full Text From Circulation with link to Free Full Text PDF Download

Part 7.5: Postresuscitation Support
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Free Full Text From Circulation with link to Free Full Text PDF Download

Footnotes were added 5/11/2011 to include links to 2010 ACLS guidelines. Links were also updated.

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Ventricular Tachycardia posts.

I have been trying to come up with a post about antiarrhythmics for sustained VT (Ventricular Tachycardia), but the abandoned drafts just pile up waiting for inspiration.

Lately, eveyone else seems to be writing about VT, so read their stuff.

Here are a few Ventricular Arrhythmia posts worth reading.

When the precordial thump works
by ER Nursey.

The precordial thump is no longer recommended by AHA, unless there is no defibrillator around. The precordial thump is supposed to act as a form of defibrillation. I have had good results with it. It seems that the precordial thump is mostly used by ICU nurses. They can see the rhythm, but the monitor does not have defibrillator capabilities. ED nurses often have not thumped anyone. ER Nursey demonstrates that she has a familiarity with the precordial thump.

Another Day on Call in the Arctic
by Albino Black Bear.

Wonderful writing. This helps to demonstrate what is meant by an austere medical environment.

Good Save
by TK.

TK mentions the counterproductive nature of OLMC (On Line Medical Command) requirements. Conversely, they initially shock VT at 50 joules, when it should be 100 joules to start for cardioversion. Perhaps that is the recommendation on this bi-phasic machine? The picture is of an old LifePak 5 with a voice recorder attachment between the paddles and the monitor. What museum provided this old picture? The first time I thumped a patient it was because of the LP5, but that is another story.

Anyway, go read these stories. Eventually, I may be able to get an antiarrhythmic post together.

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